Nouro-radiology

Neuroradiology(1991) 33:300-304

9 Springer-Verlag1991

Language disturbances from mesencephalo-thalamic infarcts
Identification of thalamic nuclei by CT-reconstructions
L. G. Lazzarino 1, A. Nicolai 1, F. Valassi 1, and E. Biasizzo 2

1 Divisionedi Neurologia,Ospedale Civiledi Gorizia,Italy
2 Serviziodi Neuroradiologia,Ospedale di Udine,Italy
Received: 29 June 1990/receivedin revisedform: 13 February1991

Summary. The authors report the cases of two patients
with CT-documented paramedian mesencephalo-thalamic infarcts, showing language disturbances. The first
patient showed a non fluent, transcortical motor-like
aphasia, the other had a fluent but severely paraphasic
language disorder. The CT study disclosed that it was the
dorso-median thalamic nucleus that was mostly involved
in both cases. These findings agree with a few previous
pathological studies suggesting that the paramedian thalamic nuclei, particularly the dorso-median nucleus may
play some role in language disturbances. However the
anatomical basis for thalamic aphasia remains speculative, taking into account the importance of cortical connections in the origin of subcortical neuropsychological
disturbances.
Key words: Thalamus - Thalamic aphasia - Mesencepha-

lo-thalamic infarcts

Several experimental and clinical studies [1-11] have
demonstrated that the most common features of thalamic
aphasia are: (1) fluent but paraphasic language, (2) relatively well preserved comprehension (3) minimally impaired or normal repetition. Sometimes non fluent language disorders can occur suggesting a transcortical
motor or sensory pattern [8-14]; in any case, the pulvinar
or the postero-lateral nuclear complex are usually involved [1-6]. However some reports [8, 9, 11,14, 15], a few
with pathological confirmation [9, 14, 15], have provided
evidence that aphasia can also be the result of paramedian
infarctions involving the thalamus of the dominant hemisphere.
In this paper we describe two right-handed patients
showing the above mentioned different aphasic patterns
caused by paramedian mesencephalo-thalamic infarcts; in
both cases several coronal and sagittal CT reconstructions
were carried out in an attempt to identify the thalamic nuclei involved in the language disorder.

Case reports

Case 1

A 72-year-old right-handed woman was admitted to hospital after being found comatose. Her previous history
was uneventful apart from mild untreated hypertension.
Blood pressure was 160/90 mmHg, the pulse rate 85
regular. Although drowsy, she was able to follow elementary verbal commands; pupils were miotic and sluggish to
light. Vertical voluntary gaze seemed completely absent,
while vertical oculocephalic movements and Bell's phenomenon were normal. In the limbs the strength, tone and
tendon reflexes were symmetrical and normal. The plantar reflexes were flexor. Tactile, pain, temperature, vibratory and postural sensations were normal. When aroused
she could execute and repeat simple orders. The spontaneous verbal output was reduced and several literal and
semantic paraphasias were evident. From two days following admission the patient was awake a comprehensive
neuropsychological evaluation could therefore be completed within three weeks of the stroke, when the patient
was sufficiently attentive. The examination started with a
careful assessment of the attention which was tested by
the Attentive Matrices and by some subtests of spatial exploration and perception (identification of superposed
configurations, identification of colours). At the moment
of the first examination attention was only slightly impaired but not enough to interfere with the language performance.
Memory and other neuropsychological functions were
explored by the Digit Span and according to Bisiach et al's
method for neuropsychological examination [16] which
are summarized in Table 1. A mild anterograde verbal
memory impairment for all modalities (serial, associative,
logical) was detected; whereas anterograde visual retrograde verbal and visual memory were well retained. Other
neuropsychological functions (spatial attention, stereognosia and praxias) were normal. Language was evaluated
according to the Boston Diagnostic Aphasia Examination
(BDAE) [17] (Table 2) after creating for it an Italian

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T a b l e 1. Examination of memory

9 Digit span
(Normal: > 5 forward,
> 3.5 backward).
Forward
Backward
9 Counting backward (20-1)
(Normal < 12 + 2 s., no errors)
Time, s.
Errors, n.
9 Learning of paired words
Easy pairs (7.5)
(Normal: 6.88 + 0.5)
9 Difficult pairs (15)
(Normal: 11.4 + 1.12)
Total: 22.5
(Normal: 18,24 + 1,17)
9 Recall of logical stories
(30)(Normal: 14.2 _+4.6)
9 Learning of 3 series
of words. (Normal: 13.8 + 3.8)

P1
3w.

4m.

3
2

5
4

4

6

3

4

25
5

14
1

20
2

12
0

5.5

6.5

5.5

7

9

10.5

10

10.2

14.5

16.5

15.5

17.2

9

12.4

9

t5.6

10

10

9

13.0

P2
2w.

6m.

onset showed a bilateral p a r a m e d i a n mesencephalo-thalamic infarction, m o r e extensive on the left side.
A formal neuropsychological evaluation was performed three weeks after admission. The attention was
evaluated by Attentive Matrices and was normal. M e m ory and other neuropsychological functions were examined by the Digit Span and according to the Bisiach
method which showed only a mild anterograde verbal
m e m o r y impairment (Table 1). No hemispatial inattention, extinction to double simultaneous stimulations, astereognosis, or apraxia were present. The B D A E showed
a fluent but severely paraphasic language, the paraphasias
being almost exclusively of semantic type. Repetition was
preserved, while comprehension was slightly impaired
(Table 2).
A neuropsychological reassessment 6 months from
onset showed no abnormalities of memory, while language disturbances, although markedly improved, were
still evident.

Methods

Neuroradiological study
scale. Fluency subtest was rated according to the guideliness of Goodglass and Kaplan and this rating was based on
a sample of conversation speech and picture description
tasks (cokie-thief) [17]. This examination showed a p o o r
verbal output with decreased articulatory agility and
phrase length, while repetition and comprehension were
normal (Table 2). A CT-scan without contrast enhancement showed a bilateral p a r a m e d i a n mesencephalo-thalamic infarction, m o r e extensive on the left side (Fig. 1).
A full reassessment 4 months after onset showed that
the m o t o r ocular disorders, attention and m e m o r y disturbances had completely cleared (Table 1) while language impairment in the form of p o o r output remained.

At least one high resolution CT-scan was p e r f o r m e d in
each patient. Prediction of vascular areas of the infarct
was based on vascular supply as described by Percheron
[18], Castaigne et al. [19] and Bogousslavsky et al. [20] and
by utilizing Damasio's templates [21].
Several reconstructions were p e r f o r m e d in coronal and
sagittal planes to identify the thalamic nuclei involved in
the infarctions. The coronal CT reconstructions were obtained with a 2 m m slice thickness in planes perpendicular
to the F o r a m e n of Monro-Posterior Commissure line
(FM-PC). C o m p u t e d rearrangement of data was obtained
in coronal planes perpendicular to the F M - P C line, beginTable 2. Results of Boston diagnostic aphasia examination

Case 2

Test category
Time

A 55-year-old right-handed m a n was hospitalized because
of abrupt onset of unresponsiveness preceded by diplopia.
His past history was good. On admission he appeared apathetic and showed a complete left third nerve palsy with
ptosis. In the right eye there was a severe limitation of upward gaze, while the downward gaze was intact. Bell's
p h e n o m e n o n was preserved and doll's head m a n e u v e r induced the upward gaze of the right eye, but no m o v e m e n t
in the left one. Pupils were equal and sluggish to light.
M o t o r examination showed a mild right hemiparesis; sensory function and coordination were intact. The patient
spoke in a whisper and fluent speech with profuse semantic paraphasias. The neurological examination was otherwise normal apart from a mild anterograde verbal m e m ory disturbance. O v e r the next few days there was a
m a r k e d i m p r o v e m e n t of consciousness while the mild
m e m o r y impairment and speech disturbances remained.
A plain high resolution CT-scan p e r f o r m e d ten days from

Fluency
9 Overall severity (0-5)
9 Articulatory agility (1-7)
9 Phrase length (1-7)
9 Grammatical form (1-7)
9 Paraphasia (1-7)

P1
3w.

P2
4m.

2w.

6m.

3
3
3
4
3

4
4
4
4
3

4
4
4
4
3

5
5
5
5
4

80
100

100
100

80
100

100
100

100
95
95

100
100
100

100
80
80

100
100
95

80
90

100
100

95
100

100
100

90
87

100
90

100
100

100
100

Auditory comprehesion %
9 Word discrimination (72)
9 Body part identification (80)
Right-left
9 Discrimination (18)
9 Commands (15)
9 Complex material (12)

Naming %
9 Confrontation (105)
9 Body part (30)

Repetition %
9 High-probability sentences (8)
9 Low-probability sentences (8)

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Fig. 1 a,b. Case 1. a Coronal CT reconstruction at the site of maximal extension of the lesion, showing a bilateral infarct of the paramedian nuclear complex of the thalamus, b Sagittal reconstruction of
the center of the lesion of the left side. Both CT reconstructions show
that the left-sided infarct involves the dorso-median nucleus, partially extending to the parafascicular, ventro-oralis and anterior nuclei

ings selected from the Schaltenbrand and Wahren's atlas
[22] and an outline of the lesion was drawn on it [23, 24].
This m e t h o d showed that in both patients the most involved thalamic structures were the dorso-median, parafascicular and ventro-oralis nuclei and, less extensively,
the anterior nuclear complex.

Fig.2a, b. Case2. a Coronal and bsagittal CT-reconstruction
showing a left paramedian thalamic infarct involving dorso-median
nucleus

Discussion

ning at the plane passing behind, by 2 m m increments, to
the anterior margin of the lesions.
Sagittal reconstructions were p e r f o r m e d on the center
of the third ventricle and on the center and lateral edge of
the lesion in the left thalamus, by using the anterior commissure-posterior commissure (AC-PC) line as reference.
The A C - P C was the line drawn between FM and the
upper point of the cerebral aqueduct. Both coronal and
sagittal reconstructions of the left thalamus were superposed on appropriate coronal and sagittal section draw-

Paramedian thalamic infarctions usually result from occlusion of small arteries originating near the basilar artery
bifurcation supplying the p a r a m e d i a n mesencephalic,
subthalamic and thalamic areas [18-20, 25-28]. The most
consistent and important are the thalamic-subthalamic
p a r a m e d i a n branchs, which originate from the proximal
posterior cerebral artery and supply the medial thalamic
nuclei, near the posterior commissure [18-20]. T h e r e may
be separate origins of the right and left thalamic-subthalamic arteries but in some cases one single pedicle on one
side can supply the p a r a m e d i a n territories on both sides
[18.20, 25-28]. This particular a r r a n g e m e n t explains how

303
a single branch occlusion can cause bilateral paramedian,
butterfly-shaped thalamic infarctions.
Infarcts in thalamo-subthalamic artery territory cause
an amnestic disorder, supranuclear gaze and nuclear
m o t o r ocular paralysis in various combinations. There
may be other cognitive and behavioral abnormalities such
as hemineglect, apathy and disinterest, particularly in patients with right-sided infarcts sometimes in the context of
"thalamic dementia" [19, 20, 24-35].
The possibility that a paramedian thalamic lesion in the
dominant hemisphere can be responsible for language disorders is disputed in the literature and there is no agreement about its clinical features [8-15, 19, 27, 28, 36]. Actually some authors deny any aphasic characteristics to
the language disorders arising form thalamic lesions [19,
36, 37] and suppose that they can m o r e closely be related
to a partial disturbance of attention involving verbal processes rather than a true aphasia [37].
The patients described herein provide further evidence
that aphasia can also be the result of lesions in the dominant p a r a m e d i a n thalamic nuclei. In addition the first patient showed a language impairment closely resembling
transcortical m o t o r aphasia: similar features have been
described after thalamic infarcts although not frequently
[8-14], while the second patient showed fluent but paraphasic language fulfilling the semiologic criteria for typical "thalamic aphasia" [4].
On the basis of clinical and CT findings in our two patients we can suggest that either the transcortical motorlike and the fluent and paraphasic language disorders can
be supported by p a r a m e d i a n ischemic lesions. In addition the CT reconstructions p e r f o r m e d in our patients
(Figs.'1,2) show that the dorso-median nucleus was involved in both cases, confirming the rare pathological findings. Since this nucleus is connected both with Broca's and
with Wernike's areas [5] we can suppose that the m o r e or
less extensive involvement of the fibres connecting these
structures may be responsible for the different aphasic features. Determining the contribution of individual thalamic
nuclei in language production is difficult since it is almost
impossible to find circumscribed damage in one region
alone. On the other hand, recent evidence suggests that in
patients with CT-verified subcortical lesions aphasia
and/or other neuropsychological disorders are associated
with cortical dysfunctions, as revealed by a cortical hypoperfusion assessed by 133 x intracarotid injection or
SPECT, and by a reduced cortical metabolism [33, 38-40].
Despite an extensive literature on language dysfunction, in
thalamic infarctions their exact anatomical and pathophysiological basis remain speculative. Further reports using
techniques of CT-reconstructions can provide some explanations on the possible role played by paramedian thalamic nuclei in the origin of language disturbances.

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